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Query: UMLS:C0021311 (Infection)
 38,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Parainfluenza 1 (Sendai) and influenza A virus pneumonitis cause severe lung damage, which, upon resolution, is followed by persistent alveolitis and parenchymal changes characterized by patchy consolidation and collagen deposition in the affected areas. To determine whether these long-term sequelae of the virus pneumonias are cumulative, mice were infected by aerosol inhalation with Sendai virus, influenza A virus, or Sendai followed 30 days later by influenza virus infection. At 90 days after the initial infection, mice were killed for assay of long-term parenchymal changes as quantitated lung hydroxyproline (Hpr) content, morphometric analysis, and total and differential lavage cell counts. Sendai virus infection did not alter the proliferation of influenza virus in the lungs as quantitated by infectious virus titers on Day 1, 3, 5, 7, 9, and 11 of influenza infection. At Day 90, lung Hpr content was cumulative in dual-infected mice, with a concomitant increase in the persistent alveolitis. To determine whether bacterial infections played a similar role in these long-term pulmonary sequelae, mice were infected by aerosol inhalation with either Staphylococcus aureus or Klebsiella pneumoniae or, during the course of influenza virus infection, superinfected with each of the bacteria. Sixty days after infection with K. pneumoniae alone, lung Hpr levels were significantly increased over those in noninfected control mice. Infection with S. aureus had no effect on the quantitated parameters of long-term lung damage. In influenza-infected mice superinfected with K. pneumoniae, lung Hpr content was significantly increased over that of S. aureus did not elevate any quantitated parameter of lung damage when compared with the virus alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sequential virus infections, bacterial superinfections, and fibrogenesis. 216 56

Infection with poliovirus effectively inhibited the translation of Vero cell messengers (carrying type 1 or type 2 caps at the 5' end) and of influenza virus messengers (type 1 caps) in co-infections. In contrast, Kunjin virus RNA (type 1 caps) and Semliki Forest virus RNA (a togavirus, with type 0 caps) continued to be translated in the presence of co-infecting poliovirus. Translation of Kunjin virus RNA was also unaffected during co-infections with either influenza virus or Semliki Forest virus. Guanidine treatment effectively blocked poliovirus replication only, but the inhibitory effect on translation of cell messengers and influenza virus messengers was still observed, indicating that this effect was not caused by competition in translation with poliovirus messengers. It was therefore concluded that the observed inhibition was most likely caused by cleavage of the p220 subunit of the cap binding protein (CBP) complex of the cell normally required for translation of capped messengers, as reported by others. However, Kunjin virus RNA could be efficiently translated apparently in the absence of a functional CBP complex, except when its secondary structure was stabilized by hypertonic salt in the culture medium.
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PMID:Successful competition in translation by the flavivirus Kunjin with poliovirus during co-infections in Vero cells. 217 65

Randomized, placebo-controlled studies with 10(3)-10(7) 50% tissue-culture infectious dose (TCID50) of avian-human (ah) and cold-adapted (ca) influenza A/Bethesda/85 (H3N2) reassortant viruses were completed in 106 seronegative young children 6-48 months of age. Although the reassortants differed in six of eight RNA segments, they exhibited similar properties in level of attenuation, infectivity, immunogenicity, and efficacy. The 50% human infectious dose was 10(4.6) TCID50 for ah and 10(4.4) for ca vaccines. Both reassortants were satisfactorily attenuated with restricted replication and were no more reactogenic than placebo. The mean peak titer of virus shed was 10(1.5) (ah) to 10(2.0) (ca) TCID50/ml, and each of 37 isolates tested retained their characteristic vaccine phenotypes. Infection with ah or ca virus conferred immunity to experimental challenge with homologous virus. These findings indicate that both ah and ca influenza A/Bethesda/85 (H3N2) reassortants should be suitable vaccine candidates for use in healthy infants and young children.
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PMID:Comparison of live attenuated cold-adapted and avian-human influenza A/Bethesda/85 (H3N2) reassortant virus vaccines in infants and children. 219 35

Knowledge of the pathogenesis of viruses which are less virulent than human immunodeficiency virus (HIV) may provide valuable insights into the pathogenesis of HIV infection. Influenza virus, an enveloped RNA virus, infects monocyte-macrophages, although the infection is brief and abortive. Isolated purified lymphocytes are completely resistant to infection. In contrast, mixtures of lymphocytes and macrophages can synthesize all virus proteins. Infection requires physical association of monocyte-macrophages and lymphocytes in "clusters." These studies with influenza virus suggest that the pathogenesis of virus infections in mixed cell cultures may be very different from that observed in purified cell populations, and they suggest that similar studies should be performed with HIV.
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PMID:Role of the monocyte-macrophage in influenza virus infection of lymphocytes: implications for HIV infection. 222 42

Infection of ferrets with influenza A virus results in a disease syndrome that is similar to that observed in humans. To examine the pathophysiology of this disease, ferrets were challenged with either H1N1 influenza virus or placebo. Sign scores and rectal temperatures were recorded periodically during the 9 days after infection. Nasal lavages were also collected during this time period and the content of kinins, histamine, cells, and total protein in these lavages was assessed. In infected animals (n = 17) compared to healthy controls (n = 14), sign scores were first significantly elevated at 30 h postinfection. Sign scores peaked at 48 to 72 h postinfection and then slowly declined, although they remained significantly elevated up to 168 h postinfection. Kinin levels were significantly correlated with signs. Associated with increased sign scores and kinins, elevations were observed in the levels of total protein and cells in nasal lavages of infected animals. In contrast to the increases in kinin levels that were observed during influenza infections, histamine concentrations in nasal lavages did not change in response to infection. We conclude that kinins are generated in nasal secretions during influenza A infections and that these potent vasoactive peptides may contribute to the symptomatology of such infections. The study of influenza infections in ferrets provides a convenient animal model in which to evaluate further the role of kinins in the pathogenesis of upper respiratory tract infections.
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PMID:Kinins are generated in nasal secretions during influenza A infections in ferrets. 236 65

An overview of the most important infections which can be transmitted from humans to pet dogs and cats is presented. Two quite different sources of infection stand diametrically opposite each other: 1. The transmission of active human infections to dogs and cats and 2. the transmission of infectious agents by feeding raw meat, offal, unsterilized milk products, kitchen scraps and contaminated feedstuffs. Humans can be the source of the following infections: 1. Zoonoses with reciprocal modes of transmission, e.g. Campylobacter and E. coli infections, trichophyton and microsporum infections, reo-, parainfluenza-, adeno, rota- and corona infections. 2. Zoonoses in which the main direction of infection is human----animal, e.g. tuberculosis and influenza A. 3. Infections originally pathogenic to humans which meet an impasse in dogs and cats (blind alley hosts), e.g. herpes simplex, varicella-zoster, measles and Corynebacterium diphtheriae. Listeria, salmonella, campylobacteria, toxoplasma, fungi, yeasts and viruses are transmitted via feed. The most dangerous virus infection to be transmitted to cats and dogs via raw pork leftovers is Aujeszky's disease. The dog or cat, which is the last link in the infection chain, suffers an agonizing death. The other infections originating from feed must be assessed quite differently. They are links in infection chains, which spread pathogens and endanger the health of man and animal in turn. A typical example is toxoplasmosis. Man becomes infected via sporulated oocysts from feces. Pet cats mainly become infected via raw pork containing cysts.
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PMID:[Infections which humans in the household transmit to dogs and cats]. 250 Aug 9

The effect of influenza virus infection on the expression of major histocompatibility complex (MHC) antigens was investigated. Infection with influenza virus resulted in an increase of the binding of anti-MHC class I and class II antibodies to resting T cells. The binding of anti-MHC class II antibodies to activated T cells was increased approximately threefold. The binding of anti-MHC class I and class II antibodies to Epstein-Barr virus-transformed B cells appeared unaffected after influenza virus infection. Recombinant human interferon-alpha and/or -gamma added to T cells did not enhance the binding of anti-MHC antibodies. Biochemical analysis revealed no increase in the amount of class I and class II antigens as a consequence of viral infection, but a marked decrease in sialic acid content was found, most probably caused by the viral neuraminidase. Pulse-chase experiments suggest that the viral neuraminidase can catalyze the removal of sialic acids both en route to and at the cell surface. The absence of sialic acid residues can explain the increased binding of anti-MHC antibodies, because neuraminidase (clostridium perfringens) treatment of T and Epstein-Barr virus-transformed B cells resulted in a shift in both isoelectric point and antibody binding similar to that observed after influenza virus infection.
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PMID:Influenza virus changes cell-surface glycoproteins including major histocompatibility complex determinants on lymphocytes. 251 59

Infection by Thogoto (THO) virus, a tick-borne virus related to the orthomyxoviruses, has been compared in vertebrate cell culture and in Rhipicephalus appendiculatus ticks using infectivity titrations, immunofluorescence, and immune electron microscopy with colloidal gold markers to detect cell surface and intracellular antigens. Morphogenesis of THO virus in cell culture was similar to that of influenza virus, with polymorphic virus particles budding at the plasma membrane. In the tick, THO viral infection caused no obvious pathology; virions or budding profiles were not observed in electron micrographs, although replication, trans-stadial persistence and transmission to a susceptible host occur. THO virus was not detected in the salivary glands of trans-stadially infected ticks until about 7 days after the commencement of feeding on a host. The synganglion (brain) appears to be the major organ involved in trans-stadial persistence of the virus; viral antigens were detected in the neural cortex (cell bodies) but not in nerve fibres and axons. The detection of THO viral antigen in basement membranes and connective tissue, but its absence from nerve fibres, suggests that dissemination occurs via the haemolymph rather than a neural route.
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PMID:Anatomical basis of Thogoto virus infection in BHK cell culture and in the ixodid tick vector, Rhipicephalus appendiculatus. 254 69

Infection with vesicular stomatitis virus (VSV) results in the rapid inhibition of cellular macromolecular synthesis, including transcription, translation, and maturation of the U1 and U2 snRNPs. Unlike infection with VSV, influenza virus infection did not result in the inhibition of either the processing of U1 and U2 snRNAs or the assembly of the RNPs. Although influenza virus relies on the cellular splicing apparatus to generate viral mRNAs, the maturation of snRNPs was inhibited during double infections with VSV. However, this inhibition of snRNP maturation had no effect on the splicing of a cellular pre mRNA in extracts prepared from VSV-infected HeLa cells. Thus, the effects of VSV on the processing and assembly of snRNPs appear to involve virus-specific functions and unique cellular targets. Coinfection with VSV and influenza virus resulted in the dramatic inhibition of influenza virus transcription; polyadenylated mRNAs corresponding to the influenza virus NP and NS1 proteins could not be detected by Northern blot analysis. However, reduced levels of the influenza virus replicative templates were still synthesized during double infection. Coinfection with VSV also resulted in the inhibition of influenza viral mRNA translation, even when superinfection with VSV was delayed until 3 or 6 hr after influenza virus infection. VSV required at least 2 hr to affect the inhibition of translation; this corresponded to the time after VSV infection when inhibition of cellular protein synthesis was evident. These results demonstrate that, in contrast to adenovirus, the VSV-mediated inhibition of cellular macromolecular synthesis may be effective against influenza virus.
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PMID:Inhibitory effects of vesicular stomatitis virus on cellular and influenza viral RNA metabolism and protein synthesis. 254 15

In the spring term of 1985 there was a protracted outbreak of upper respiratory tract febrile illness consistent with a clinical diagnosis of influenza in a boys' boarding school, which lasted from 23 January to 29 March. Although influenza virus infection was confirmed in 89% of cases in the first half of the term, 53% of the cases which occurred in the second half of the term had no evidence of infection with influenza virus. Between 5 February and 31 March 28 boys presented with skin rashes consistent with a clinical diagnosis of erythema infectiosum; 68% of these were associated with parvovirus B19. Investigation of the cases of clinical influenza with no identified respiratory pathogen revealed a 58% infection rate with B19. B19 DNA was identified in either throat swabs or acute stage bloods of nine pupils with influenza-like symptoms. Cohort studies revealed that 44% of pupils aged 15-16 years were immune before the outbreak compared with only 17% of pupils aged 11-12 years. Infection in the younger group was common and was associated with influenza-like illnesses as well as rashes. Forty-eight per cent of those who did not report any symptoms were also infected with B19.
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PMID:Concurrent outbreaks of influenza and parvovirus B19 in a boys' boarding school. 255 64


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